Osteoporotic spinal compression fractures are associated with significant performance impairments in physical, functional, and psychosocial domains.
Most are isolated fractures of the anterior spinal column related to low bone mineral density.
Postmenopausal women and patients taking long-term corticosteroid therapy are most susceptible.
The causative mechanism is a combination of flexion and axial compression loading.
It is important to exclude the possibility of pathologic fracture due to malignancy or infection.
Treatment frequently involves pain relief, temporary use of an orthosis (e.g., Jewett/Lumbar brace or thoracolumbosacral orthosis) and walking aids (e.g., stick, elbow crutches, all-terrain rollator).
Radiographic and clinical follow-up is required every 6 weeks for 3 months post-injury.
Most osteoporotic spinal compression fractures represent an isolated failure of the anterior spinal column due to a combination of flexion and axial compression loading. The stability of the spine is not compromised with this type of fracture. These fractures are traditionally considered benign injuries that heal without complications. Rarely, osteoporotic compression fractures can also involve the middle and/or posterior spinal columns, in addition to the anterior column. This type of fracture is potentially unstable and requires surgical intervention.
History and exam
- older age (>50 years for women and >65 years for men)
- previous osteoporotic vertebral compression fracture
- low body weight
- recent weight loss
- family history of low bone mass/osteoporotic fractures
- white or Asian race
- postmenopausal status
- secondary amenorrhea
- alcohol (>2 units/day)
- corticosteroid use
- glucocorticoid excess
- vitamin D deficiency
- low calcium intake
- rheumatoid arthritis and other autoimmune connective tissue diseases
- endocrine disorders (e.g., hypogonadism, hyperparathyroidism, hyperprolactinemia, acromegaly, hypercortisolism, hyperthyroidism)
- gastrointestinal diseases (e.g., inflammatory bowel disease, celiac disease, malabsorption syndromes, post-bariatric surgery)
- liver diseases (e.g., biliary sclerosis, sclerosing cholangitis, alcoholic cirrhosis, autoimmune hepatitis)
- dietary disorders (e.g., anorexia nervosa/bulimia, inadequate diet, total parenteral nutrition)
- neurologic disorders (e.g., stroke, multiple sclerosis, Parkinson disease, spinal cord injury, long-term immobilization)
- renal disease
- type 1 diabetes mellitus
- organ transplantation
- bone-losing medications
Nasir A. Quraishi, LLM, FRCS
Consultant Spine Surgeon & Honorary Clinical Associate Professor
Centre for Spinal Studies and Surgery
Queen’s Medical Centre
NAQ declares that his institution has received research support from Medtronic.
Opinder Sahota, FRCP, DM, FHEA
Professor of Orthogeriatric Medicine & Consultant Physician
Queen's Medical Centre
Nottingham University Hospitals NHS Trust
OS declares that he has no competing interests.
Jeremy Fairbank, MD, FRCS
Professor of Spine Surgery
University of Oxford
Nuffield Orthopaedic Centre
JF declares that he has no competing interests.
Sheldon Jacobson, MD, FACP, FACEP
Department of Emergency Medicine
Mount Sinai School of Medicine
SJ declares that he has no competing interests.
Micky Malhotra, MBBS, DTCD, MD, MRCP
Wrightington, Wigan & Leigh NHS Foundation Trust
MM declares that he has no competing interests.
Use of this content is subject to our disclaimer